Role of NO in reduction of myocardial ischemia-reperfusion injury by ginsenoside Rb1 preconditioning in diabetic rats

Abstract

Objective To evaluate the role of by NO in reduction of myocardial ischemia-reperfusion （IR）injury by ginsenoside Rb1 preconditioning in diabetic rats. Methods Forty healthy adult male SD rats weighing 220-280 g were used in this study. Diabetes mellitus was induced by intraperitoneal streptozotocin 65 mg/kg and confirmed by fasting blood glucose 〉 16.7 mmol/L. The animals were randomly divided into 4 groups （ n = 10each）： sham operation group （group S）, group IR, ginsenoside Rb1 group （group R） and L-NAME ＋ ginsenoside Rb1 group （group LR）. IR was produced by occlusion of the anterior descending branch of left coronary artery （LAD） for 30 min followed by 120 min reperfusion in group IR, R and LR. In group S, LAD was exposed but not occluded. In group LR, L-NAME 10 mg/kg was injected iv 25 min before ischemia. In group R and LR, ginsenoside Rb1 40 mg/kg was injected iv 10 min before ischemia. In group S and IR, eaqual volume of normal saline was injected instead of ginsenoside Rb1. The blood sample was taken from carotid artery at 120 min of reperfusion for determination of serum activities of creatine kinase （CK） and lactate dehydrogenase （LDH）. Then the animals were sacrificed and myocadial tissues were obtained for determination of infarct size, endothelial nitric oxide synthase （eNOS） expression, MDA and NO contents, SOD activity and microscopic examination. Results The serum activities of CK and LDH were significantly increased and the myocardial infarct size was enlarged in group IR, R and LR, and eNOS expression was significantly down-regulated, MDA content was increased, and SOD activity and NO content was significantly decreased in group IR and LR compared with group S （ P 〈 0.05）. The serum activities of CK and LDH, and MDA content were significantly decreased, the myocardial infarct size was reduced, the expression of eNOS was up-regulated and the activity of SOD was increased in group R compared with group IR and LR （ P 〈 0.05）. There was no significant difference in the indices mentioned above between group IR and LR （ P〉 0.05）. Conclusion Ginsenoside Rb1 preconditioning can attenuate myocardial IR injury in diabetic rats via activation of eNOS, increase in NO production, and inhibition of the lipid peroxidation reaction. Key words: Nitric oxide; Ginsenosides; Ischemic preconditioning; Diabetes mellitus; Myocardial reperfusion injury